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. 2017 Jun 1;9(1):83–98. doi: 10.1080/21505594.2017.1326443

Figure 5.

Figure 5.

4E-BP1 is a downstream effector of PI3K-Akt-mTOR signaling in sustaining rotavirus infection. (A) Western blot assay detected t-Akt and t-4E-BP1 (53H11) in lentiviral RNAi against 4E-BP1 transduced Caco2 cells. (B) Knockdown of 4E-BP1 significantly inhibited SA11 rotavirus genomic RNA quantified by qRT-PCR (n = 5, mean ± SEM, *P < 0.05, Mann-Whitney test). (C) Anti-rotavirus effect of rapamycin (10 nM) was abolished in 4E-BP1 knockdown Caco2 cells (n = 5, mean ± SEM, *P < 0.05, **P < 0.01, Mann-Whitney test). (D) Western blot assay confirmed that anti-rotavirus effect of rapamycin (10 nM) was abolished in 4E-BP1 knockdown Caco2 cells. (E) Western blot indicated bona fide knockdown of 4E-BP1 in knockout (−/−) MEF cells. (F) SA11 rotavirus replication was potently restricted in 4E-BP1 knockout (−/−) MEF cells (n = 4, mean ± SEM, *P < 0.05, Mann-Whitney test). (G) Anti-rotavirus effect of rapamycin (10 nM) was attenuated in 4E-BP1 knockout (−/−) MEF cells (n = 8, mean ± SEM, *P < 0.05, Mann-Whitney test). (H) Rapamycin inhibited rotavirus replication in 4E-BP1 KO MEFs transfected with 4E-BP1-WT plasmids; while this antiviral effect was abolished in 4E-BP1 KO MEFs transfected with 4E-BP1–5A plasmids (n = 5, mean ± SEM, *P < 0.05, Mann-Whitney test).